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DOCK2 in Disease: Emerging Insights and Research Advances
Zhaolong Yu1,2, Songzhi Jin1,2,3, Shujing Wan1,2
1Key Laboratory of Innate Immunity and Chronic Inflammatory Diseases, Jiangxi Provincial Department of Education, Gannan Medical University, Ganzhou, China.
Background:
This review aims to synthesize the structural and functional characteristics of DOCK2, as well as its mechanistic roles in various diseases, in order to provide a theoretical foundation for targeted therapies.
Methods:
We systematically reviewed existing literature to summarize the molecular features and expression patterns of DOCK2, its regulation of cellular processes through both Rac-dependent and Rac-independent pathways, and its implications in inflammation, cancer, fibrosis, and related disorders.
Results:
DOCK2, a member of the Dock-A subfamily of GEFs, is widely expressed across tissues and prominently in immune cells (e.g., dendritic cells, macrophages, T cells, B cells), where it regulates proliferation, differentiation, migration, and cytokine secretion primarily via Rac activation. Emerging evidence also links DOCK2 to non-immune cell types such as glial cells and vascular smooth muscle cells, highlighting its relevance in immune-related and broader pathological conditions including inflammatory diseases, cancer, atherosclerosis, idiopathic pulmonary fibrosis, and obesity.
Conclusion:
As a critical GEF, DOCK2 plays a central role in immune and non-immune cellular processes through Rac and non-Rac signaling pathways. Dysregulation of DOCK2 is closely associated with multiple diseases. Further elucidation of its regulatory networks may reveal novel therapeutic targets for treating related disorders.
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